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Palmitic Acid Activates c-Myc via Dual Palmitoylation-dependent Pathways to Promote Colon Cancer

GSE299569 Mus musculus (mouse) RNA-seq (gene expression) 26 samples Submitted 2026/02/25 Platform GPL24676Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 26 samples

What it is
RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism
Mus musculus (mouse)
Topic
Colorectal cancerThis series is part of our curated briefing on it.
Samples
26 samples: 7 conditions, mostly with about 5 replicates eachGroups are read from the sample names, not from the paper. Check the list below.
Data you can get
A processed table (series matrix) and supplementary files from NCBI; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.
Paper
Palmitic acid activates c-Myc via dual palmitoylation-dependent pathways to promote colon cancerCell discovery · 2026
Summary (written by the submitters)
Transcriptional factor c-Myc plays a crucial role in various types of cancer including colon cancer. c-Myc is hyperactivated during the tumorigenesis and malignant progression of colon cancer, but the mechanisms underlying this transcriptional activation remain largely unknown. Considering that colon cancer is constantly exposed to intestinal metabolites, we wonder whether they play a key role in c-Myc transcriptional activation.
Read the full summary ↓
Here, we reveal that palmitic acid is essential for the transcriptional activation of c-Myc during both inflammation-driven tumorigenesis and tumor progression. Notably, c-Myc is activated by palmitic acid in dual palmitoylation-dependent pathways  “passive activation under palmitic acid exposure” and “proactive activation through palmitic acid uptake”. Finally, exploiting metabolic addiction to palmitic acid as a vulnerability, we propose a promising therapeutic strategy inhibiting palmitoyltransferase ZDHHC9 and fatty acid transporter FATP2 which exerts favorable therapeutic effects against colon cancer. Together, these findings not only uncover a crucial biological role of palmitic acid on c-Myc activation depending on palmitoylation at distinct stages of colon cancer, but also highlights targeting ZDHHC9 and FATP2 as a promising option for colon cancer treatment.
Published in
Palmitic acid activates c-Myc via dual palmitoylation-dependent pathways to promote colon cancer
Du W, Zhang J, Wang Y et al. · Cell discovery 2026 · PMID 41698889 · doi:10.1038/s41421-026-00869-6
This dataset
Open GSE299569 in finder → Find more RNA-seq datasets → Colorectal cancer landscape →
Download · which file do I need?

Direct links to NCBI and ENA, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.

1 · Just have a look

Processed table

The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.

Series matrix ↓
2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE299569_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓
3 · Start from the raw reads

Raw sequencing reads

The original FASTQ files, straight from the sequencer, held at ENA. Large, and you align them yourself, so only choose this if you need to re-process the study from scratch.

Raw reads on ENA ↗

What the files usually look like: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJNA1274998 and SRA study SRP591442. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41698889) ↗
Study design
7 conditions, mostly with about 5 replicates each
colonic tissue derived from DSS-treated C57B… ×5 colonic tissue derived from DSS-treated C57B… ×5 colonic tissue derived from DSS-treated C57B… ×5 colonic tissue derived from DSS-treated C57B… ×3 HCT116 subcutaneous xenograft in nude mice su… ×3 HCT116 subcutaneous xenograft in nude mice su… ×3 colonic tissue derived from DSS-treated C57BL… ×2

Supports a between-group comparison across 26 samples.

How we read this: 7 replicated groups read from 26 sample titles; they account for 26 of them. These groups are guessed from the sample names, not taken from the paper, so check them against the sample list below before relying on them.

Samples in this study
More Colorectal cancer datasets

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